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Brain and Behaviour 2 > Clinical Neuroscience > Flashcards

Clinical Neuroscience Flashcards

1
Q

The parietal lobe

A
  • This part of the brain’s ‘vision-for-action’ stream (dorsal stream)
  • Receives input from the V1 (primary visual cortex)
  • Key functions:
    1) Space based attention
    2) Object based attention
    3) Reaching and grasping
    4) Magnitude processing
    5) Feature based attention
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2
Q

Neuropsychological disorders of the parietal lobe

A
  • Damage to the parietal lobe can results in a wide range of neuropsychological disorders
  • These disorders depend on the location and hemisphere of the lesion
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3
Q

Neuropsychological disorders of the parietal lobe: hemispatial neglect

A
  • This occurs as a result of damage to the right parietal lobe
  • Patients don’t attend to the left side of space
  • But they can attend when objects are pointed out to them
  • This means that neglect is not a problem in the visual cortex
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4
Q

Right vs left damage and neglect

A
  • Neglect is much more common in the right compared to the left hemisphere
  • Right hemisphere is dominant for visuo-spatial attention
  • Right hemisphere represents both contralateral and ipsilateral space
  • Left hemisphere represents contralateral space only
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5
Q

Summary of impairments in hemispatial neglect

A
  • Patients neglect objects/people/environment in the left visual field
  • They also have problems imagining the left visual field
  • Patients can attend to objects in the left visual field when they are directed to them
  • This pattern of impairments shows that neglect is a problem with attention and not with perception
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6
Q

Neglect in the audio domain

A
  • Neglect patients may sometimes respond to voices/sounds originating from the affected hemispace as if they occurred from the ipsilesional side of space
  • Neglect patients show poorer audio location compared to patients with right brain damage without neglect. These deficits are specific to the contralesional side of space
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7
Q

Bálint’s syndrome: key symptoms

A
  • The result of bilateral damage to parietal and occipital lobes
  • 3 distinct impairments:
    1) Simultanagnosia (inability to perceive multiple objects simultaneously)
    2) Optic ataxia (difficulty reaching for objects due to spatial misjudgment)
    3) Oculomotor aproxia (impaired eye movement planning)
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8
Q

Goodale et al (1994): dorsal vs ventral pathway

A
  • Investigated the effects of dorsal vs ventral visual stream damage on object perception
    Patient RV (dorsal steam damage):
  • Bilateral parietal lobe lesions impacting the dorsal ‘where’ pathway
  • Abilities: could perceive the shapes of objects. Was mostly able to distinguish between the presented shaped
  • Deficits: significant errors in reaching and grasping, particularly in targeting objects’ orientation and position
    Patients DF (ventral stream damage):
  • Bilateral ventral occipital lesions affecting the ventral ‘what’ pathway
  • Abilities: could physically interact with objects (grasping successfully)
  • Deficits: poor shape perception; performed at chance when identifying objects’ shapes

This highlights the functional specialisation of the dorsal and ventral pathways in visual processing:
- Dorsal (where pathway): responsible for spatial awareness and visually guided actions
- Ventral (what pathway): responsible for object recognition and identification

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9
Q

Optic ataxia

A
  • A disorder associated with impaired visually guided movements, typically caused by damage to the parietal lobe (dorsal stream, ‘where pathway’)
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10
Q

Oculomotor apraxia

A
  • A problem making planned and purposeful eye movements
  • Patients have problems and saccade initiation and accuracy, and smooth visual pursuit
  • May happen in patients with Bálint’s syndrome due to deficits in a circuit between the parietal lobe and frontal eye fields
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11
Q

Dyscalculia: a disorder of magnitude processing

A
  • This is developmental disorder, caused by acquired damage, usually referred to as ‘acalculia’
  • Patients tend to have a problem understanding and manipulating numbers (e.g arithmetic, multiplication etc)
  • Prevalence estimates around 3-6%
  • Neuroimaging studies suggest that the deficit is localised in the right inferior parietal lobule
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12
Q

Price et al (2007): numerical distance effect

A
  • The idea that it is easier to identify the larger of two numbers when there is a greater numerical distance between them
  • 8 children with developmental dyscalculia and 8 controls completed a numerical distance effect task during an FMRI scan
  • Controls showed greater activations within right intra parietal sulcus when working with close or far number distances
  • Children with DD did not shows this effect
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13
Q

A theory of magnitude (ATOM)

A
  • Time, space and number all require us to compare size or magnitude
  • Time, space and number share a common neural underpinning in the right intraparietal sulcus
  • Time, space and number share a common neural substrate in the right intraparietal sulcus
  • Similar cognitive functions are likely to be processed in the same brain area
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14
Q

Major depressive disorder (MDD) is diagnosed if 5 or more of these behaviours are present

A
  • Depressed mood
  • Reduced interest in pleasure (Anhedonia)
  • Significant weight change
  • Disturbed sleep (insomnia/hypersomnia)
  • Abnormal motor activity
  • Fatigue, tiredness, or loss of energy
  • Feelings of worthlessness of excessive guilt
  • Diminished ability to think or concentrate
  • Recurrent suicidal ideas (with or without a plan)

Each symptom is a complex behavioural pattern, involving multiple malfunctioning brain areas

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15
Q

Beck’s cognitive model of depression

A
  • In this model, depressive symptoms are generated and maintained by combination of of maladaptive cognitions
  • Individuals with depression are said to be prone to:
    1) Selectively attend to negative stimuli (biased attention)
    2) Experience greater awareness/perception for negative stimuli (biased processing)
    3) Ruminate about depressive ideas (biased thought and rumination)
    4) Recall depressive episodes with more frequency (biased memory)
    5) Possess negative internal reps about about the self and environment (negative schemas)
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16
Q

A cognitive neuroscience model of depression

A

1) Vulnerability:
- Genetic
- Personality
2) Environmental triggers:
This results in schema activation:
- Biased attention (increased and sustained amygdala)
- Biased processing (increased amygdala reactivity to negative stimuli, increased thalamic activity, blunted NA and caudate nucleus responses to positive stimuli)
- Biased memory and rumination (increased amygdala activity correlated with increased hippocampal, caudate and putamen activity, which in turn predicts recall of negative information

Biased attention > biased processing > biased memory
3) Depressive symptoms

A number of different brain regions that are involved in depression which can be mapped to the different cognitive patterns thought to trigger and sustain a depressive episode

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17
Q

Biased attention in depression

A
  • Amygdala important for recognition and generation of emotion
  • In healthy controls, attention is generally biased towards positive stimuli, whereas individuals with depression instead show ban attentional bias for negative stimuli
  • Problems allocated attention could contribute dysphoria
    Brain regions associated with attention include:
  • Parts of the parietal cortex
  • Prefrontal cortex
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18
Q

Siegle et al (2007): an increased emotional response to negative stimuli

A
  • Used fMRI with unmedicated depression patients and healthy controls during two tasks:
    1) A digit sorting task (cognitive)
    2) A personal relevance ratings of words task (emotional)
  • Patients with depression showed increased amygdala activity for negative words, and decreased DLPFC for all tasks
  • So a negative emotional response is stronger and less well regulated by top down-brain areas involved in attention allocation
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19
Q

Biased in processing in depression

A
  • Reward processing affected in depression
  • Reward in the brain is supported by a frontostriatal network, neural pathways that connect frontal lobe regions with the basal ganglia (striatum)
  • Nucleas accumbens (NAcc) is part of the reward network- it is a major input to the striatum (basal ganglia)
  • Disruption in this network has been argued to be the basis for anhedonia
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20
Q

Heller et al (2009): altered brain responses during emotion regulation

A
  • Examined brain responses during emotion regulation paradigm via fMRI
  • Participants were instructed to enhance or suppress emotional response to positive or negative images, or simply to attend
  • The depression sample failed to sustain NAcc activation when amplifying
  • Deficits in sustaining activity in the NAcc were specific to positive emotion
  • Patients who fail to sustain NAcc activity report less intense positive emotion
  • Difficulties sustaining NAcc activation reflect reduced prefrontal connectivity
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21
Q

Biased memory in depression

A
  • Increased awareness for negative stimuli influences likelihood that negative information will be encoded and later recalled
  • Activity in the amygdala facilitates the encoding and retrieval of emotional stimuli in healthy individuals by modulating brain regions associated with memory
  • Biased memory in depression is associated with amygdala hyperactivity, which is positively correlated with activity in the hippocampus, caudate and putamen
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22
Q

Videbech and Ravnkilde (2004):

A
  • Conducted a meta analysis of studies examining hippocampal volume in patients with MDD
    They found:
  • A significant reduction in hippocampal volume was observed in patient with MDD compared to healthy controls
    The extent of volume reduction correlated with:
  • Duration of illness
  • Number of depressive episodes

The hippocampus is crucial for memory formation, regulation of emotional responses and stress adaptation

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23
Q

The neurotrophic hypothesis of depression: cause or consequence?

A
  • Human post-mortem data shows decreased BDNF in hippocampus
  • Impairs memory encoding
  • Demonstrates neuroplasticity at a very specific autonomical level
  • Not clear if this is a cause or consequence of depression
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24
Q

Three classes of neurochemical implicated in depression

A

1) Glucocorticoids (mainly cortisol in humans)
2) Brain derived neurotrophic factor (BDNF)
3) Monoamines (dopamine, serotonin, noradrenaline)

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25
Q

Cortisol

A
  • A steroid hormone, increases blood sugar, suppresses immune system, increases metabolism
  • Increased cortisol raises performance during stress
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26
Q

Brain derived neurotrophic factor (BDNF)

A
  • BDNF maintains and supports growth of neurons/synapses
  • Expressed in many brain areas but especially related to memory formation in the hippocampus
  • Relates to the neurotrophic theory of depression
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27
Q

Monoamines

A
  • Monoamines are neurotransmitters that are released to send signals to other neurons:
    1) Dopamine: reward and motivation, supports approach and consummatory behaviours. It is released from the ventral tegmental area (VTA) to forebrain networks
    2) Serotonin: ‘happiness’ molecule but also many complex behaviours (e.g dominance). It is released from dorsal raphe to forebrain networks
    3) Noradrenaline: ‘fight or flight’ molecule that prepares the body for action. It is released to organs all over the body
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28
Q

Monoamine treatments

A
  • Have to overcome homeostatic feedback mechanisms
  • Many different side effects (e.g insomnia, aggression, suicidal thoughts etc)
  • Effects can wash-out over time
  • Should not be a single treatment but as a part of a treatment programme
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29
Q

The monoamine theory of MDD

A
  • In the healthy brain, monoamine neurotransmitters are released and bind to receptors on the postsynaptic neuron. Transmission is terminated by re-uptake of transmitter
  • In depression, there is decreased concentration of monoamine at synaptic sites
  • Treatment could involve the blockage of the re-uptake sites to increase the concentration of monoamine neurotransmitters available at receptor sites to restore mood
30
Q

The scale of the pharmacological problem: STAR*D trial (2006)

A
  • STAR*D is a large-scale study testing the efficiency of antidepressant treatments across increasing levels of intervention
  • They aimed to understand how different treatment combinations affect remission rates in MDD
    Level 1: SSRI for 14 weeks to assess initial treatment response
    Level 2: switched to different SSRIs or added CBT optionally
    Level 3: switched to alternative antidepressants
    Level 4: switched to SNRIs or MAOIs (monoamine oxidase inhibitors)
  • They found that 70% of participants who completed all levels achieved remission
  • Withdrawal rates increased at each treatment level, reflecting the burden of prolonged or intensive treatment regimens
  • Certain groups (e.g women, wealthier, better educated) had better responses overall
31
Q

The genetics of MDD

A
  • MDD is highly heritable (50% chance of parent diagnosed)
  • MDD more heritable in women than men
  • We all have at least some of the genes that correlate with MDD
  • The extent to which we have genes that cause MDD varies
32
Q

Wray et al (2018): hot spot genetic locations for MDD

A
  • 44 variants argued to map onto 19 genetic pathways to depression
  • This can be used identify likelihood of depression developing
  • Using polygenic sequencing to compare an individual’s DNA to the roadmap in order to estimate how likely one is to develop depression at some point in their life
33
Q

The role Gene SLC6A4 plays in causing MDD

A
  • This gene regulates the expression and transportation of serotonin in the brain
34
Q

Genes and environment in MDD: Caspi et al (2003)

A
  • Investigated the interaction between genetic predisposition and environmental factors (stressful life events) in contributing to MDD risk
  • Genetic focus was on the 5-HTTLPR genotype, related to serotonin transport
  • Participants were grouped based on their genotype:
    1) s/s homozygotes (short-short variants)
    2) s/l heterozygotes (short-long variants)
    3) l/l homozygotes (long-long variants)
  • Environmental measure: number of stressful life events experienced
    Results:
  • They found that the gene allele variant does not independently cause MDD
  • Gene-environment interaction: individuals with the s/s genotype and a higher number of early-life events had a significantly increased risk of MDD. Those with l/l genotype showed lower susceptibility to stress-induced depression

The risk of MDD is thus an output of both one’s genetic predisposition and one’s environment

35
Q

Genetics impact brain structure

A
  • Voxel brain morphometry (VBM) used to measure gray matter volume of 5-HTT gene
  • Carriers of the short allele (s/s) variation show reduced volume in amygdala and perigenual cingulate
  • Connectivity between amygdala and cingulate impaired in 5-HTT group when viewing fearful stimuli
36
Q

Post traumatic stress disorder (PTSD)

A
  • Normal to experience upsetting/confusing thoughts after a traumatic event, but in most people these naturally improve over a few weeks
    The symptoms/criteria for PTSD include:
  • A stressor event
  • Intrusion symptoms
  • Alterations in arousal/reactivity
  • Negative alterations in cognition/mood
  • Avoidance behaviours
    Complex PTSD- trauma related to multiple events over an extended period of time
37
Q

Criteria for PTSD diagnosis

A

1) Stressor
2) Alterations in arousal and reactivity
3) Intrusion symptoms
4) Negative alterations in mood
5) Avoidance
- Symptoms last for more than 1 month
- Symptoms create distress or functional impairment
- Symptoms are not due to medication

38
Q

Amygdala

A
  • This is part of the limbic system
  • Emotion processing (of all kinds)
  • Component of the reward, motivation and learning networks
  • Stimulates the HPA-axis
39
Q

Liberzon et al (1999): Amygdala and PTSD

A
  • PTSD veterans, combat veterans and controls scanned with PET whilst either white noise was played or combat sounds
  • PTSD veterans showed greater stress and skin response to combat noise than white noise
  • PTSD veterans showed a greater response to combat noise in left amygdala
40
Q

Cingulate cortex

A
  • Anterior cingulate cortex (ACC)
  • Involved in attention, reward, decision making and emotion
  • Part of the frontal-striatal network
  • Also part of the ‘salience network’, involved in altering attention to threats/unexpected stimuli
41
Q

Shin et al (2001): Atypical ACC responses in PTSD

A
  • 8 war veterans with PTSD vs 8 war veterans without PTSD
  • Subjects counted the number of combat words, negative words and neutral words
  • Results showed a diminished response to negative in ACC
  • ACC mediates/controls response to negative stimuli in healthy brain
42
Q

Thalamus

A
  • The brain’s relay station for sensory information
  • Thalamus responds to bottom-up and top-down input
  • The hypothalamus forms a key part of the HPA axis
43
Q

Dorsolateral prefrontal cortex

A
  • Greater bold activity when controlling cognitive response
  • Part of frontal-striatal network
44
Q

Orbitofrontal cortex (also called ventromedial prefrontal cortex)

A
  • OFC involved in decision making and future planning
  • Also task switching and evaluation
  • On the pathway between DLPFC and the amygdala
45
Q

Hippocampus

A
  • Part of the limbic system
  • Memory processing
  • Attenuates the HPA-axis
46
Q

Etkin and Wagner (2007): meta analysis of PTSD

A
  • Compared fMRI studies of PTSD, social anxiety and phobias
  • Patients with any of these disorders showed grater activity than matched comparison subjects in the amygdala and insula
  • PTSD specifically showed hypoactivity in OFC, thalamus and cingulate
47
Q

Logue et al (2019): hippocampus and PTSD

A
  • Meta analysis of 1868 patients (794 PTSD patients)
  • Smaller hippocampus = increased chance of PTSD
48
Q

Gilbertson et al (2002): hippocampus and PTSD twin study

A
  • MZ twin study examined if hippocampal volume was the cause or result of trauma
  • Combat veterans
  • Results showed hippocampal volume predicted severity of PTSD in the combat exposed twin and non-combat exposed twin
  • Smaller hippocampus increases likelihood of mental illness
  • They concluded that hippocampus size was a risk factor and not a result of trauma
49
Q

The neurotrophic hypothesis of depression

A
  • Could the involvement of the hippocampus be due to depression rather than PTSD
  • Human post-mortem data shows decreased BDNF in hippocampus
  • Impairs memory encoding
  • Demonstrates neuroplasticity at a very specific anatomical level
  • It is not clear if this is a cause or a result of depression
50
Q

The hypothalamic-pituitary adrenal-(HPA) axis

A
  • The HPA axis is a key system coordinating the neuroendocrine response to stress:
    1) A stress stimuli is detected causing neurons in the hypothalamus release CRH
    2) This stimulates the production and release of ACTH from the anterior pituitary
    3) This ACTH hormone then stimulates the release of glucocorticoids (including cortisol) from the adrenal gland
51
Q

The role of glucocorticoids in HPA

A
  • They modulate metabolism, immune response and brain function
  • They also prepare the body for fight or flight
52
Q

Brain regulation of the HPA axis

A
  • Inhibitory pathways: hippocampus and PFC reduce HPA axis activity
  • Excitatory pathways: amygdala stimulates hypothalamic neurons, increasing HPA axis activity
53
Q

HPA axis in PTSD

A
  • Several studies suggest differences in regions like the hippocampus and amygdala, which helps to regulate the HPA axis
  • Some studies suggest cortisol is actually reduced in PTSD, possibly due to negative feedback effect
  • Some studies suggest subtypes of PTSD differ with regards to their cortisol/HPA reactivity
  • There are multiple ways to measure cortisol which may be the source of the confusion
54
Q

Sleep disturbances in PTSD

A
  • Insomnia
  • Nightmares (trauma replay)
  • Disruptive nocturnal behaviours: night terrors, sleep paralysis, dream enactment
  • Longer sleep latency
  • More awakenings during the night
  • Shorter total sleep time
55
Q

Cortical hyperarousal in PTSD

A
  • Maladaptive levels of arousal throughout the day and night
  • Pre-sleep arousal includes intrusive thoughts when falling asleep
  • During sleep, beta oscillations are a marker of cortical hyperarousal
  • Patients with PTSD show signs of increased cortical hyperarousal throughout the night
56
Q

Does sleep prospectively predict PTSD

A
  • Studies in military personnel have measured sleep prior to development and found that those who developed PTSD following trauma showed disturbed sleep before developing PTSD
57
Q

Sleep supports (emotional) memory consolidation

A
  • Sleep preferentially strengthens emotionally charged experiences
  • Sleep deprivation impairs memory and emotion regulation
  • Sleep to remember, sleep to forget
58
Q

Treatment of PTSD using cortisol

A
  • Hydrocortisone is a steroid that works as a hormone replacement cortisol
  • There have been some studies on the possibility of using hydrocortisone for treating PTSD
  • Kothgassner et al (2021) suggest hydrocortisone helps as a preventative measure after trauma against PTSD, but does very little if PTSD has already developed
59
Q

Extinction

A
  • This means by which a fear response can be inhibited
  • Heavily studies in animal literature (e.g Pavlov)
  • Offers a behavioural and neural explanation of why CBT works
  • Extinction is a form of learning, it is not ‘unlearning’
  • Extinction = learning new skills
60
Q

Extinction in the brain

A

1) Ventral medial prefrontal cortex (or OFC)
- Greater activity in the vmPFC is associated with enhanced extinction learning (better)
- It signals the amygdala to reduce and regulate the fear response
2) Dorsal lateral cingulate cortex (dACC)
- Activity negatively correlates with extinction learning
- Higher dACC activity is associated with poorer extinction learning due to it’s involvement in maintaining fear response
3) Amygdala
- The primary centre for fear and threat responses
- Extinction learning reduces it’s activation, mediated by signals from the vmPFC

Improved connection between vmPFC and dACC leads to better extinction outcomes due to improved fear regulation

61
Q

Extinction as an analogue for exposure therapy

A
  • Exposure therapy is one of the main psychological therapies for PTSD
  • Also used for treating phobias, panic disorder, social anxiety etc
  • It involves the therapist creating a safe environment to expose patients to the thing they fear:
    1) Directly facing a feared object or situation
    2) Imagined exposure
    3) Virtual reality
    4) Written exposure
  • Sleep may enhance exposure therapy as well as promoting successful extinction retention
62
Q

EMDR: eye movement desensitisation and reprogramming

A
  • Developed by Shapiro (1989)
  • The patient follows with their eyes rapidly moving stimulus while holding different aspects of traumatic events in mind
  • Systematic reviews of RCTs suggest that it is effective
63
Q

EMDR: neurobiological hypotheses

A
  • One theory is that EMDR is related to memory processes
  • PTSD could be considered a consequence of failed memory processing, arising when brain fails to consolidate or integrate an episodic memory, leading to continued maintenance of the memory and feelings associated with it
  • It imitates REM sleep as this stage is associated with memory consolidation
64
Q

Acquired brain injury

A
  • This a broad term that refers to damage to the brain that a child was not born with. It is the result of an accident/event that happened later:
    1) Traumatic brain injury: caused by something happening outside the body e.g head injury
    2) Non-traumatic injury: cause by something going on inside the body e.g stroke
65
Q

What is a stroke?

A
  • A stroke occurs when blood flow to an area of the brain is cut off
  • There are a number of physiological reasons for this occurring
  • When blood flow is restricted, brain cells are deprived of oxygen, leading to cell death
66
Q

Two main types of stroke

A
  • Ischemic stroke: when arteries to the brain become blocked/narrow, this causes severely reduced blood flow
  • Haemorrhagic stroke: when blood vessels in brain leak/rupture
67
Q

Risk factors of strokes in children and adults

A
  • In both adults and children, ischemic strokes are the most common, but the risk factors are different:
    1) Children:
  • Cardiac problems, especially congenital heart disease, or following surgery
  • Sickle cell disease: an inherited condition that affects the development of red blood cells
  • Serious infections
    2) Adults:
  • Hardening of arteries
  • Diabetes
  • High blood pressure
68
Q

Warning signs of a stroke

A

For newborns/infants:
- Seizures
- Extreme sleepiness
- Tendency to use only one side of body
For children/teens:
- Severe headaches
- Vomiting
- Sleepiness
- Dizziness
- Loss of balance/coordination

69
Q

Long-term outcomes of stroke in children: Christerson and Stromberg (2010)

A
  • Follow-up of 51 children who had suffered strokes:
    1) mortality: 4 of them died
    2) Neurological deficits: the majority of those surviving had lasting neurological impairments. Hemiparesis (weakness on one side of the body) was a common outcome
    3) Educational impact: most faced school activity deficits
    -
70
Q

Anderson et al (2013): effect of strokes on social abilities

A
  • Compared social competence of children who’d had arterial ischemic stroke (AIS) vs controls and children with asthma
  • AIS children had more social problems than controls
  • Lesion volume not related to social outcomes
  • Younger age at stroke predicted better social interaction and higher self-esteem

Brain and Behaviour 2 (4 decks)

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